Document Type : Original Article
Authors
1
Student Research Committee, Gonabad University of Medical Sciences, Gonabad, Iran
2
Department of Biochemistry, School of Medicine, Gonabad University of Medical Sciences, Gonabad, Iran
3
Clinical Research Development, Unit of Tabriz Valiasr Hospital, Tabriz University of Medical Sciences, Tabriz, Iran
4
Department of Anatomy, School of Medicine, Gonabad University of Medical Sciences, Gonabad, Iran
5
Department of Obstetrics and Gynecology, School of Medicine, Allameh Bohlool Gonabadi Hospital, Gonabad University of Medical Sciences, Gonabad, Iran
6
Department of Physiology, School of Medicine, Gonabad University of Medical Sciences, Gonabad, Iran
Abstract
Background: Minocycline is a widely used bacteriostatic antibiotic with various functions. The aim of this study was
to investigate impact of apoptotic genes in ovary of the torsion/detorsion treated rat model by minocycline.
Materials and Methods: This experimental study was performed in 32 female Wistar rats classified in four groups,
including: i. sham, ii. TD: torsion/detorsion group received normal saline, iii. TDM: torsion/detorsion group treated
with 40 mg/kg Minocycline, and iv. MC: healthy group received 40 mg/kg Minocycline. After treatment period (7
days), histoplogical parameters, oxidative stress markers and hormone profile of serum as well as the expression of
Bax and Bcl-2 genes were measured in the ovary of rats.
Results: Levels of superoxide dismutase (SOD), glutathione peroxidase (GPX) and estrogen were decreased in the
TD group and significantly increased in the treated groups (P=0.001). Levels of malondialdehyde (MDA) and testosterone
were increased in the TD group and decreased in the treated groups (P=0.001). Expression level of Bax was
elevated in the TD group, while it was attenuated in the treated groups (P=0.001). Expression level of Bcl-2 was
significantly increased in treated groups (P=0.001).
Conclusion: Minocycline can repair oxidative damage in ovarian tissue and regulate apoptotic-related gene expressions.
Keywords